Ameliorating effect of leukotriene receptor antagonist in multi-organ toxicity induced in rat offspring, a possible role for epidermal growth factor.

Purpose: Nowadays, there is a dramatic increase in the interest of potential impact of consumer-relevant engineered nanoparticles on pregnancy.Materials and methods: This study investigated the possible protective effect of montelukast in neonatal organ toxicity induced by maternal exposure to silver nanoparticles (AgNPs) in rats.Results: It was noticed that montelukast reduced serum urea, creatinine, renal caspase-3 immunoreactivity and IL-1ß and increased total antioxidant capacity, as compared to AgNPs. In kidney and bone tissue, montelukast reduced oxidative stress parameters and TNF-α level that was increased with AgNPs. Surprisingly, montelukast administration increased epidermal growth factor (EGF) in bone and reduced it in kidney. Furthermore, as compared to AgNPs, montelukast improved histopathological picture of kidney and bone.Conclusions: In conclusion, montelukast antagonized the biochemical and histopathological changes occurred in kidneys and bones of rat offspring by maternal exposure to AgNPs, mostly by anti-oxidant, anti-apoptotic and anti-inflammatory actions with a possible role for EGF.

The protective effect of fenofibrate, triptorelin, and their combination against premature ovarian failure in rats.

Cyclophosphamide (CP) is a chemotherapy alkylating agent that causes a lot of side effects including premature ovarian failure (POF). This study aimed to evaluate the possible protective effect of fenofibrate (FEN) in CP-induced POF. Rats were randomly divided into five groups as follows: negative control, CP, triptorelin (TRI)-treated, FEN (FEN)-treated, and FEN + TRI-treated. Histological study, collagen area fraction, and immunoexpression of proliferating cell nuclear antigen (PCNA) were evaluated. Also, estrogen, anti-mullerian hormone (AMH), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and ovarian malondialdehyde (MDA), nitric oxide (NOx), reduced glutathione (GSH), superoxide dismutase (SOD), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and vascular endothelial growth factor (VEGF) were measured. CP significantly reduced ovarian follicle count, as compared with the control group (1.00 ± 0.76 versus 7.75 ± 1.83, respectively). Meanwhile, FEN, either solely or in combination with TRI, significantly increased ovarian follicle count, as compared with the CP group (3.88 ± 0.83 and 5.75 ± 1.39, respectively). As compared with the control group, CP increased the levels of MDA, NOx, IL-10, TNF-α, FSH, LH, and collagen area fraction; however, levels of GSH, SOD, VEGF, AMH, estrogen, and PCNA immunoexpression were reduced with CP. Administration of FEN either solely or in combination with TRI showed significant improvement in all the parameters previously mentioned. FEN can protect the ovary from CP-induced side effects possibly through antioxidant and anti-inflammatory actions.

Ameliorative effect of nicorandil in ovarian ischemia-reperfusion-induced injury in rats: role of potassium channel.

Ovarian torsion is a gynecological emergency that leads to serious outcomes. Nicorandil (NIC) is an ATP-sensitive potassium (KATP) channel activator that protects the heart from ischemia. The current study aimed to investigate the role and mechanism of action of NIC in ovarian ischemia-reperfusion (OIR) and possible KATP participation. Twenty-four female albino rats were classified into 4 groups: sham control, OIR, OIR + NIC, OIR + NIC+ glibenclamide (GLB) groups. Serum anti-Müllerian hormone (AMH), ovarian malondialdehyde (MDA), total nitrites (NOx) contents, and superoxide dismutase (SOD) activity were evaluated. Bax and Bcl2 mRNA were also assessed. Histological and immunohistochemical (anti-COX-2 and anti CD68) studies were done. The OIR non-treated group showed histopathological ovarian injury with decreased AMH level. Ovarian MDA, NOx, and Bax mRNA and the expression of COX-2 and CD68 were increased; however, SOD activity and Bcl2 mRNA level were decreased by OIR. NIC significantly ameliorated the histopathological ovarian injury with the restoration of AMH level. NIC significantly corrected oxidative stress and apoptotic biomarkers with decreased COX-2 and CD68 immunostaining. GLB co-administration significantly decreased the protection afforded by NIC. These results imply that NIC has a protective role against OIR via antioxidant, anti-inflammatory, and anti-apoptotic effects and such protection relies, at least partially, on the KATP channel.

Possible protective effect of royal jelly against cyclophosphamide induced prostatic damage in male albino rats; a biochemical, histological and immuno-histo-chemical study.

Almost all the chemotherapy treat many cancer types effectively, but it leads to severe side effects. Chemotherapy like cyclophosphamide (CP) not works only on the active cells, such as cancer cells, but also acts on the healthy cells. Royal jelly (RJ) was reported to have a lot of therapeutic effects besides being an anti-oxidant and anti-cancer agent. The purpose of this study was to assess the possible protective role of RJ in ameliorating the toxic effects of CP overdose in the rat prostatic tissue. The rats were separated into 4 groups; control group, RJ group, CP group and RJ with CP group. Prostatic specimens were processed for biochemical, histological and immune-histo-chemical studies. The mean area fractions of eNOS and Bax expression were measured in all groups, and statistical analysis was carried out. The results showed that in CP treated group, there were marked biological changes in the form of significant increase in prostatic malondialdehyde (MDA) and C - reactive protein (CRP). Additionally there was a significant decrease in glutathione peroxidase (GPx) in prostatic tissue if compared with the control group. Furthermore, the histological changes showed marked acinar and stromal prostatic degeneration. Most prostatic acini showed less PAS reaction and more (eNOS and Bax) expression if compared with the control group. Concomitant administration of RJ with CP revealed a noticeable amelioration of these biochemical and histological changes. In conclusion, RJ provided biochemical and histo-pathological improvement in CP induced prostatic tissue toxicity. These findings revealed that this improvement was associated with a decrease in the tissue oxidative damage and apoptosis.